Nuclear receptor coregulator NRIP1 R448G modulates T cell gut homing to control intestinal inflammation

Nuclear receptors (NRs) are crucial to integrate metabolite sensing and immune responses in the gut. NR-interacting protein 1 (NRIP1) is an important coregulator of various NRs that has been implicated in inflammatory bowel disease risk, but mechanistic details of how NRIP1 controls NR activities mediating immune homeostasis and inflammation remain elusive. We demonstrate that a missense risk variant, NRIP1 R448G, promotes activated CD4<sup>+</sup> T cell gut homing and inflammatory cytokine production, ultimately leading to exacerbated intestinal inflammation. Mechanistically, NRIP1 acts as a corepressor in retinoic acid signaling by expression of a gut-homing transcriptional program. Our study reveals the impacts of NRIP1 on CD4<sup>+</sup> T cells in immune regulation during intestinal inflammation, providing insights into mechanisms by which an NR coregulator controls immune homeostasis and tissue inflammation.

Authors

Institutions

Publication Details

Journal
Proceedings of the National Academy of Sciences
Published
2025-09-18
DOI
https://doi.org/10.1073/pnas.2508269122
Primary Topic
Immune Cell Function and Interaction
Type
article
Field-Weighted Citation Impact
0.00
Controls
|||
ALL TIME
JAN
FEB
MAR
APR
MAY
JUN
JUL
AUG
SEP
OCT
article

Nuclear receptor coregulator NRIP1 R448G modulates T cell gut homing to control intestinal inflammation

Yanhua Zhao, Elizabeth A. Creasey, Daniel B. Graham, Orr Ashenberg et al.
Proceedings of the National Academy of Sciences
Immune Cell Function and Interaction
article

Nuclear receptor coregulator NRIP1 R448G modulates T cell gut homing to control intestinal inflammation

Yanhua Zhao, Elizabeth A. Creasey, Daniel B. Graham, Orr Ashenberg, Lei Deng, Ramnik J. Xavier, Bihua Li, Han Sung Hwang, Xiangjun Chen, Koushik Ghosh
article en

Abstract

Nuclear receptors (NRs) are crucial to integrate metabolite sensing and immune responses in the gut. NR-interacting protein 1 (NRIP1) is an important coregulator of various NRs that has been implicated in inflammatory bowel disease risk, but mechanistic details of how NRIP1 controls NR activities mediating immune homeostasis and inflammation remain elusive. We demonstrate that a missense risk variant, NRIP1 R448G, promotes activated CD4<sup>+</sup> T cell gut homing and inflammatory cytokine production, ultimately leading to exacerbated intestinal inflammation. Mechanistically, NRIP1 acts as a corepressor in retinoic acid signaling by expression of a gut-homing transcriptional program. Our study reveals the impacts of NRIP1 on CD4<sup>+</sup> T cells in immune regulation during intestinal inflammation, providing insights into mechanisms by which an NR coregulator controls immune homeostasis and tissue inflammation.

Proceedings of the National Academy of SciencesVol. 122(38)
Broad Institute (US), Brigham and Women's Hospital (US), Harvard University (US), Massachusetts General Hospital (US)
Openalex Percentile: Top 73%
Immune Cell Function and Interaction
AI Navigator

Ask Laika to Summarize, Analyze, and Connect papers live on the map.

Summarize Papers & Methodologies

Extract key findings, datasets, and comparative methods across publications.

Benchmark Rankings & Visual Analytics

Rank top research institutions, authors, funders, topics, and journals by Field-Weighted Citation Impact (FWCI) and paper volume with instant charts.

Connect Distant Disciplines

Bridge topological clusters on the map to find hidden collaborative intersections.